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Rapid tomcod ‘evolution by pollution’? Yeah, right … and wrong

Published: 22 February 2011 (GMT+10)

Joanie Côté, Wikipedia.org
The Atlantic tomcod only benefits from its information-losing mutation in the heavily
polluted Hudson River.

Headlines have screamed that fish in New York’s Hudson River have ‘evolved’
into ‘super mutants’, able to resist the toxic effects of PCBs (polychlorinated
biphenyls) in that heavily polluted waterway. And all this ‘evolution’
has happened in less than 50 years.1

As reported in the respected journal Science,2 researchers have indeed shown that some 95% of the
Hudson’s bottom-feeding Atlantic tomcod have become resistant to these poisons.
It is the first recorded case of poison resistance (similar to antibiotic resistance
or pesticide resistance) developing in vertebrates (creatures with backbones). And
this is almost certainly via mutation, which is then favoured by natural selection.

Why would the same article that made those frank admissions about these damaged,
weakened fish have a headline that referred to them as having ‘evolved’
into ‘super mutants’?

So the fish have adapted to this new environment by a Darwinian mechanism. But as
we have already extensively shown in detail (for example, in
this article on supergerms), such resistance to poisons in bacteria, for
instance, most definitely does not demonstrate the sort of biological change
required to have turned microbes into magnolias, mosquitoes and microbiologists.
It is in fact demonstrating the opposite, if anything, especially in those cases
of antibiotic resistance where mutations have generated the resistance.

This is something that is simple to understand and demonstrate; the germs become
resistant due to various forms of damage (which is what mutations—inherited
genetic copying mistakes—mostly do) to their internal engineering. A good
example is where a germ that uses biological pumps to draw in its nutrition has
a mutation that damages the pumps. That makes it harder for it to pump in not just
nutrients, but also antibiotics when these are in its environment—in short,
it is no longer as good at sucking in the poison that kills it.

So the ones that have this defect do better when there are such poisons
around (natural selection—a fact of life). But they are ‘damaged goods’,
unable to pump in nutrients as efficiently—so, once the poison is removed
from their surroundings, they don’t do as well as the normal, undamaged germs.
So the ‘normal’ type of germ will come to dominate the population once
more, because it is more efficient at what it needs to do.

This is not ‘evolution’ (as most people understand that word to mean)
at all, since that requires a net uphill gain of information, improvements giving
greater viability and efficiency, building new and improved biological machinery,
not damaging that which exists. In short, even a committed evolutionist should concede
that this sort of mutation that ‘breaks things’ is not the sort that
he would like to see to demonstrate the viability of his belief in ‘uphill’
evolution.

And—surprise, surprise—despite the media hype, all indications are that
the same sort of downhill damage as in the bacterial example just given has taken
place in the case of the Hudson tomcod. All such Atlantic tomcod fish have a gene
called AHR2. This codes for a receptor protein which in its normal state allows
PCBs to bind to it, causing severe problems (some 30 years ago, 94% of Hudson tomcods
were found to have a PCB-induced liver tumour, for instance). The Hudson River variety,
according to one of the researchers, Dr Mark Hahn of the Woods Hole Oceanographic
Research Institution, “appear to be missing two of the 1,104 amino acids normally
found in this protein”. This is apparently the result of six of the bases
in the gene’s DNA sequence having been deleted (two lots of three bases, each
coding for one amino acid).

This loss mutation has damaged the receptor such that PCBs and dioxins cannot bind
as readily to it. Mutation happens in one generation, and since in such a poison-rich
environment the non-damaged fish would be rapidly eliminated, it’s no wonder
(and in keeping with other instances in non-vertebrates of poison resistance) that
the mutated gene would spread quickly enough to dominate the population in just
a few decades.

Given that these mutant fish are ‘damaged goods’, and in keeping with
our comments earlier, it’s also no surprise to read about the Hudson tomcod
that “the fish have suffered in other ways. They likely grow slower than other
tomcod, and they may have reduced resistance to other dangers.”3

One would therefore expect that these genetically damaged fish would not do as well
in less polluted areas, and so again it’s no surprise to read that only “5%
of the fish in the nearby, relatively clean waters off Connecticut and Long Island
possess the mutated gene.”

Of course. About the only surprise is, why would the same article that made those
frank admissions about these damaged, weakened fish have a headline that referred
to them as having “evolved” into “super mutants”?

But then, maybe one shouldn’t be surprised there, either. It seems that in
this day and age sensationalist headlines that keep reinforcing the idea that there
is all this ‘evidence’ of ‘evolution happening’ are just
par for the course. If anything, it should encourage us all to get involved much
more with passing on the sort of information that can counter this ‘propaganda
war’; tell your friends and acquaintances about this site; subscribe to our
free email newsletter; give them gift subscriptions to Creation magazine, hand out
books and DVDs
of quality creation information. And keep yourself informed. Yes, it helps us to
keep going and growing, but it is also one way in which all of us can ‘do
our thing’ to help combat this relentless onslaught of misinformation. As
you get behind us, we can ‘make the bullets’ in this spiritual war,
but we need you to help fire them.

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